Reduced transfer of tetanus antibodies with placental malaria

Me, Brair; Brabin, Bernard; Milligan, Paul; Maxwell, S. M.; Ca, Hart

doi:10.1016/s0140-6736(94)90991-1

Cited by 114 publications

(53 citation statements)

References 4 publications

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“…To do this, we used a Luminex-bead-based assay that allowed us to measure antibodies to EBV lytic (e.g., VCA-p18, VCAgp125, EAd, and Zta) and latent (e.g., EBNA1) antigens as well as TT antigen (13). We included the TT antigen as a reference antigen, as there are numerous studies evaluating the transplacental transfer of anti-TT antibody (22,26,34,35). The levels of EBVspecific anti-VCA-p18, anti-VCA-gp125, and anti-TT antibodies were comparable in the mothers and their neonates irrespective of malaria exposure status (Fig.…”

Section: Resultsmentioning

confidence: 99%

“…A number of conditions are known to affect the maternal-fetal transfer of IgG antibodies, including HIV infection, placental malaria, and maternal hypergammaglobulinemia (23,26,27,34). In this study, only HIV-negative mothers were enrolled, and we adjusted for hypergammaglobulinemia in our multivariate analysis, with results indicating that the effect of reduced transfer of anti-VCA-p18 and anti-EBNA1 antibodies was likely due to maternal malaria infection during pregnancy.…”

Section: Discussionmentioning

confidence: 99%

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Reduced Transplacental Transfer of a Subset of Epstein-Barr Virus-Specific Antibodies to Neonates of Mothers Infected with Plasmodium falciparum Malaria during Pregnancy

Ogolla

Daud

Asito

et al. 2015

Clin Vaccine Immunol

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h Over 35% of children in a region of malaria endemicity are infected with Epstein-Barr virus (EBV) by 6 months of age. This susceptibility may be linked to impaired transplacental transfer of antibodies. In this study, we determined the effect of malaria exposure during pregnancy on the transfer of EBV-specific maternal antibodies in a region of western Kenya that experiences endemic malaria. Pregnant mothers were recruited and followed up until delivery to determine levels of neonatal malaria exposure. Levels of EBV lytic (viral capsid antigen [VCA], Z transcriptional activator [Zta], and early diffuse antigen complex [EAd]) and EBV latent (EBV nuclear antigen-1 (EBNA1]) and tetanus-specific IgG antibodies were measured in 70 paired maternal and cord blood samples using a Luminex-bead-based assay. A high proportion (63%) of the infants were exposed to malaria in utero. Levels of EBV-and tetanus-specific antibodies were similar in malaria-infected mothers and in mothers who had no detectable malaria infection. Malaria-exposed neonates had significantly lower levels of anti-EBNA1, anti-Zta, and anti-EAd antibodies than were seen in their mothers. In utero malaria exposure resulted in significant reductions in transplacental transfer of anti-VCA-p18 and anti-EBNA1 antibodies of 13% and 22%, respectively. Neonates received significantly low levels of anti-Zta and anti-EAd antibodies irrespective of malaria exposure levels. In multivariate analysis, in utero malaria exposure was associated with a significant reduction in the transfer of anti-VCA-p18 and anti-EBNA1 antibodies to the neonates (P ‫؍‬ 0.0234 and P ‫؍‬ 0.0017, respectively). Malaria during pregnancy results in differential levels of transfer of EBV-specific antibodies from the mother to the fetus. The impaired transplacental transfer of some antibodies may lead to the malaria-exposed neonates being susceptible to early EBV infection. E ndemic Burkitt's lymphoma (eBL) is a distinct form of nonHodgkin's lymphoma and is the most common pediatric malignancy in regions of malaria endemicity of sub-Saharan Africa (1). Both infection with Epstein-Barr virus (EBV) and repeated episodes of Plasmodium falciparum malaria are known risk factors for eBL (2), but the mechanism(s) by which these two agents interact to promote the emergence of malignant B cell clones has not been elucidated. Recently, we found that infants from a region of malaria endemicity of western Kenya were infected with EBV by 6 months of age (3). Living in regions of malaria endemicity was a predictor of this early age of primary infection. This aberrant primary EBV infection may set the stage for lymphoma development, as previously hypothesized (4-6).The lytic and latent phases of the EBV life cycle induce distinct antibodies in response to specific lytic and latent antigens. Anti-EBV nuclear antigen-1 (EBNA1) antibodies are produced against EBNA1, the only antigen expressed in latently infected memory B cells and in eBL tumors (7). Anti-viral capsid antigen (anti-VCA), anti-early antigen (ant...

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Reduced Transplacental Transfer of a Subset of Epstein-Barr Virus-Specific Antibodies to Neonates of Mothers Infected with Plasmodium falciparum Malaria during Pregnancy

Ogolla

Daud

Asito

et al. 2015

Clin Vaccine Immunol

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“…The transplacental IgG transport involves a connection to the Fc receptor on the surface of syncytiotrophoblast [24], however, some clinical conditions such as maternal HIV infection, malaria, prematurity and maternal hypergammaglobulinemia may interfere with this transport, but we did not observe reports of changes in the placental passage of antibodies in malnourished pregnant women [25][26][27][28][29].…”

mentioning

confidence: 76%

Placental transfer of Haemophilus influenzae type b antibodies in malnourished pregnant women

Cavalcante¹,

Kopelman²,

Costa‐Carvalho³

2008

Braz J Infect Dis

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This study evaluated the vaccination response to Haemophilus influenzae type b (Hib) in malnourished pregnant women (MN), cord blood (CB) and in infants at two and six months of age for comparison with a control group (C). Twenty-eight malnourished pregnant women and 29 pregnant controls were immunized with conjugated Act-HIB® in the third trimester of pregnancy. Blood samples were collected from all before the immunization, during labor (post immunization), and from CB. All infants were immunized with Hib vaccine according to normal vaccine schedule and sera were collected at two and six months of age. Antibody levels to polyribosylribitol phosphate (PRP) were similar for both groups. Preimmunization: MN 1.94 μ μ μ μ μg/mL, C 1.68 μ μ μ μ μg/mL; post-vaccination: MN 18.53 μ μ μ μ μg/mL and C 17.55 μ μ μ μ μg/mL; in CB from MN 14.46 μ μ μ μ μg/mL and from C 17.04 μ μ μ μ μg/mL. Infants from MN and C mothers presented respectively at two months: 5.18 μ μ μ μ μg/mL and 8.60 μ μ μ μ μg/mL and at six months: MN 3.42 μ μ μ μ μg/mL and C 2.18 μ μ μ μ μg/mL.Antibody levels were similar in both groups studied (p = 0.485), however the vertical transmission rate was 14% lower in the MN pregnant group. Levels of antibodies ≥ ≥ ≥ ≥ ≥ 0.15 μ μ μ μ μg/mL were found in all newborns from the MN pregnant group. Pregnant MN presented an immunological response to Hib vaccine similar to group C, however, vertical transmission rate of antibodies to PRP in the MN pregnant group was 14% lower than that in C, suggesting a less efficient passage of antibodies within this group.

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“…3,9 ± 11 Parasitic involvement of the placenta also impedes passive antibody transfer to the fetus. 12 Even after delivery, women who have contracted falciparum malaria during pregnancy are at increased risk for the development of ARDS, possibly secondary to the increase blood volume associated with delivery. 3,9,10 The placenta is usually involved in patients with falciparum malaria; microscopic examination of the placenta are just as sensitive, and possibly more sensitive than concurrently obtained thick blood preparations for the diagnosis of malaria in patients from endemic areas.…”

Section: Clinical Perinatal/neonatal Case Presentationsmentioning

confidence: 99%

Persistence of Plasmodium falciparum in the Placenta After Apparently Effective Quinidine/Clindamycin Therapy

et al. 2001

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A 19-year-old pregnant woman, who recently immigrated to the United States from West Africa presented to the hospital with complaints of nausea, vomiting, recent diarrhea, and lower abdominal pain. She was a 34.4-week primapara and reported that her symptoms began several days before admission and were increasing in severity. The patient reported no significant past medical history. She had not taken malaria prophylaxis, as directed by her physicians in Liberia.Her physical examination on admission demonstrated a jaundiced, febrile (101.68F), gravid female in moderate distress. Vital signs disclosed tachypnea (36 bpm), tachycardia (130 bpm), and a blood pressure of 128/70 mm Hg. Her right lower abdominal quadrant was not tender to palpation and rebound tenderness was not present. The cervix was not effaced. Fetal monitoring demonstrated uterine contractions, without significant decelerations.Laboratory findings showed elevated bilirubin and liver enzymes, a significant pancytopenia, with a leukopenia (1940 WBCs/cumm) and left-shifted hematopoiesis (34% bands), thrombocytopenia (17,000 platelets/cumm), and a diminished hemoglobin and hematocrit (8.4 g/dl and 24.1%, respectively). A peripheral smear confirmed the pancytopenia, showed schistocytes, and disclosed Plasmodium-infected erythrocytes. The parasite was promptly determined to be Plasmodium falciparum and the parasitemia was determined to be 3%. The patient was treated with a combination of quinidine and clindamycin (quinidine gluconate 500 mg intravenous (IV) loading dose, followed by a continuous infusion at 1.0 to 1.2 mg/min; clindamycin 900 mg IV every 8 hours), because she had immigrated from a region where chloroquine-resistant P. falciparum strains have been reported. The antiplasmodial therapy resulted in a rapid decrease in peripheral parasitemia and subsequent elimination of plasmodia from the circulation. The patient was concurrently stabilized by packed red blood cell and platelet transfusions. She underwent cesarean section delivery secondary to nonreassuring fetal heart tones, with late decelerations and failure of the delivery to progress. At the time of delivery, the patient had received 22.5 hours of quinidine/clindamycin, with almost complete clearance of plasmodia from the peripheral circulation; extremely rare parasites were detected only after an exhaustive search. The infant was delivered without complications and did not develop malaria.Histopathologic examination of the placenta demonstrated extensive sequestration of P. falciparum-infected erythrocytes in the maternal sinuses, with a local parasitemia of 70% to 80% ( Figure 1). Other histopathologic findings, which have been associated with malaric placentas were also present, including fibrin deposition and abundant malarial pigment within placental histiocytes. Rare plasmodia were detected in the fetal circulation of the placenta. The child was treated and did not develop malaria.Several maternal and neonatal peripheral blood smears, obtained during the postpartum period, were ne...

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Reduced transfer of tetanus antibodies with placental malaria

Cited by 114 publications

References 4 publications

Reduced Transplacental Transfer of a Subset of Epstein-Barr Virus-Specific Antibodies to Neonates of Mothers Infected with Plasmodium falciparum Malaria during Pregnancy

Reduced Transplacental Transfer of a Subset of Epstein-Barr Virus-Specific Antibodies to Neonates of Mothers Infected with Plasmodium falciparum Malaria during Pregnancy

Placental transfer of Haemophilus influenzae type b antibodies in malnourished pregnant women

Persistence of Plasmodium falciparum in the Placenta After Apparently Effective Quinidine/Clindamycin Therapy

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